Our mathematical/computational Preliminary Studies emphasize the analysis of experimental data collected by our multidisciplinary team at Center of Cancer Systems Biology in conjunction with human data from the literature, to construct a predictive model of dynamic steps in carcinogenesis Initiation consists of one or more comparatively rapid genomic or epigenetic alterations; the alterations produce cell clones that may become dysplastic or hyperplastic and are at risk for being transformed. Promotion, according to one common view, involves the proliferation of initiated, and thus premalignant, cells. Promotion may take many years and the cell lineages may incur additional alterations. (Malignant) transformation is a further genomic or epigenetic alteration in an initiated/promoted lineage. Sometimes, transformation is considered to be one point mutation in a key gene, but other models consider larger scale DNA changes (e.g. deletions, duplications, translocations and inversions, aneuploidy, or horizontal transfer) and/or consider multiple alterations instead of just one alteration. Progression occurs as a malignant cell lineage evolves in interaction with its microenvironment, often becoming increasingly malignant and invasive. Genomic instability is a common feature. Many computational models implement all or part of this timeline, often with additional steps (reviewed, e.g., in [Cox & Huber 2007; Little et al. 2008a]). One basic implementation is the classic two-stage clonal expansion (TSCE) model, which emphasizes probabilistic promotion. Two-stage refers to initiation to pre-malignancy (stage 1) and transformation to malignancy (stage 2).